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Osteoking prevents bone loss and enhances osteoblastic bone formation by modulating the AGEs/IGF-1/β-catenin/OPG
Yi Yang1, Rong Li1, Peijin Wang1
1Department of Laboratory Animal Science, Kunming Medical University, Kunming, China.
Abstract:
Type 2 diabetic osteoporosis (T2DOP) is a skeletal metabolic syndrome characterized by impaired bone remodeling due to type 2 diabetes mellitus, and there are drawbacks in the present treatment. Osteoking (OK) is widely used for treating fractures and femoral head necrosis. However, OK is seldom reported in the field of T2DOP, and its role and mechanism of action need to be elucidated. Consequently, this study investigated whether OK improves bone remodeling and the mechanisms of diabetes-induced injury. We used db/db mice as a T2DOP model and stimulated MC3T3-E1 cells (osteoblast cell line) with high glucose (HG, 50 mM) and advanced glycation end products (AGEs, 100 µg/mL), respectively. The effect of OK on T2DOP was assessed using a combined 3-point mechanical bending test, hematoxylin and eosin staining, and enzyme-linked immunosorbent assay. The effect of OK on enhancing MC3T3-E1 cell differentiation and mineralization under HG and AGEs conditions was assessed by an alkaline phosphatase activity assay and alizarin red S staining. The AGEs/insulin-like growth factor-1(IGF-1)/β-catenin/osteoprotegerin (OPG) pathway-associated protein levels were assayed by western blot analysis and immunohistochemical staining. We found that OK reduced hyperglycemia, attenuated bone damage, repaired bone remodeling, increased tibial and femoral IGF-1, β-catenin, and OPG expression, and decreased receptor activator of nuclear kappa B ligand and receptor activator of nuclear kappa B expression in db/db mice. Moreover, OK promoted the differentiation and mineralization of MC3T3-E1 cells under HG and AGEs conditions, respectively, and regulated the levels of AGEs/IGF-1/β-catenin/OPG pathway-associated proteins. In conclusion, our results suggest that OK may lower blood glucose, alleviate bone damage, and attenuate T2DOP, in part through activation of the AGEs/IGF-1/β-catenin/OPG pathway.
Insights
Osteoking (OK) may treat type 2 diabetic osteoporosis (T2DOP) by lowering blood glucose and repairing bone remodeling. This study found OK activates the AGEs/IGF-1/β-catenin/OPG pathway, improving bone health in T2DOP models.
Area of Science:
- Biomedical Sciences
- Endocrinology
- Orthopedics
Background:
- Type 2 diabetic osteoporosis (T2DOP) is a metabolic bone disease linked to type 2 diabetes mellitus, with current treatments having limitations.
- Osteoking (OK) is used for bone conditions like fractures but its role in T2DOP is largely unexplored.
- Understanding OK's mechanism in T2DOP is crucial for developing new therapeutic strategies.
Purpose of the Study:
- To investigate the efficacy of Osteoking (OK) in improving bone remodeling in a type 2 diabetic osteoporosis (T2DOP) model.
- To elucidate the underlying molecular mechanisms by which OK exerts its effects on diabetes-induced bone injury.
- To assess OK's impact on osteoblast differentiation and mineralization under high glucose and advanced glycation end product conditions.
Main Methods:
- Utilized db/db mice as a T2DOP model and MC3T3-E1 cells stimulated with high glucose (HG) and advanced glycation end products (AGEs).
- Assessed OK's effects on bone remodeling using mechanical bending tests, H&E staining, and ELISA.
- Evaluated osteoblast differentiation and mineralization via ALP activity and Alizarin Red S staining; analyzed protein expression of the AGEs/IGF-1/β-catenin/OPG pathway using Western blot and immunohistochemistry.
Main Results:
- Osteoking (OK) treatment reduced hyperglycemia, attenuated bone damage, and repaired bone remodeling in db/db mice.
- OK increased tibial and femoral IGF-1, β-catenin, and OPG expression while decreasing RANKL and OPG expression.
- OK promoted MC3T3-E1 cell differentiation and mineralization under HG and AGEs conditions, modulating key pathway proteins.
Conclusions:
- Osteoking (OK) demonstrates potential in treating type 2 diabetic osteoporosis (T2DOP) by alleviating hyperglycemia and bone damage.
- OK's therapeutic effects appear to be mediated through the AGEs/IGF-1/β-catenin/OPG signaling pathway.
- Further research into OK as a treatment for T2DOP is warranted, given its positive impact on bone remodeling and cellular processes.
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